Maturation of the corpus callosum of the rat: I. Influence of thyroid hormones on the topography of callosal projections.
The normal adult rat corpus callosum contains numerous axonal profiles that are immunoreactive for the high molecular weight subunit of the neurofilament triplet (NF-H). NF-H immunoreactivity develops gradually during the first 2 postnatal weeks. The expression of NF-H immunoreactivity is almost completely suppressed in rats rendered hypothyroid by neonatal treatment with propylthiouracil. To ensure that the cytoskeletal deficit was due to a shortage of thyroid hormones rather than to unspecific, toxic effects of propylthiouracil, hypothyroid animals kept on the propylthiouracil diet were given restorative thyroxine injections daily. Such animals express NF-H at normal levels. This suggests that the callosal axons may be arrested at an immature stage of development. The immaturity of the hypothyroid corpus callosum can also be revealed by a comparison of the myelin content in the corpus callosum between normal rats, hypothyroid rats, and hypothyroid rats under thyroxine therapy. Hypothyroid rats are severely deficient in myelin, and again this deficit can be corrected by postnatal thyroxine treatment. During normal callosal development, there is a progressive spatial restriction of the transcallosal projection that creates in the adult patches of callosally projecting cortex interposed by acallosal regions. Given the structural immaturity of the hypothyroid callosal axons, it was interesting to investigate the state of development of their topography. For this purpose, multiple injections of wheat germ agglutinin-horseradish peroxidase were made into the occipital and parietal cortices of adult hypothyroid animals. In normal rats, the majority of visual callosally projecting cells are located in three groups--in area 18b, at the boundary of area 17 and 18a, and in the lateral portion of area 18a. Within these areas projecting cells are concentrated in layers II-III, Va, and Vc-VIa. The callosal axon terminals are concentrated in these same regions, with a laminar distribution as far as the somata plus layer I. In the midportion of areas 17 and 18a, fewer callosal cells are found, and they occupy mainly layers Vc-VIa, as in the case for terminals in these same areas. In the parietal cortex, callosal cells and terminals are disposed in vertical arrays alternating with almost empty zones. Most are concentrated in layers III and V. The topography of the callosal axon terminal fields is unaffected by hypothyroidism. However, there is a dramatic redistribution of the callosally projecting cell somata.(ABSTRACT TRUNCATED AT 400 WORDS)
Gravel
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C
Department of Biochemistry, Faculty of Medicine, Laval University, Quebec, Canada.
Hawkes
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R
D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology* / Q000254:growth & development; D003337:Corpus Callosum / Q000166:cytology / Q000254:growth & development / Q000378:metabolism*; D003599:Cytoskeleton / Q000502:physiology*; D007037:Hypothyroidism / Q000139:chemically induced; D007150:Immunohistochemistry; D007382:Intermediate Filaments / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013963:Thyroid Hormones / Q000502:physiology*; D014498:Uracil / Q000031:analogs & derivatives
D013963:Thyroid Hormones; C056698:6-n-propyluracil; D014498:Uracil